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Year 3 Cardiovascular pathology (Pathology (congenital (Semilunar valve…
Year 3 Cardiovascular pathology
Pathology
congenital
Shunted flow - congenital defects
Clinical signs - developing signs of cardiac failure poor exercise intolerance, cyanosis, coughing and stunted body growth).
causes
• Single or multiple gene defects.
• Chemicals (thalidomide, ethanol), toxins, physical agents (irradiation, hypoxia), nutritional deficiencies (vit A, Zinc).
Ectopia cordis
Congenital development of the heart at an abnormal site
outside of the thoracic cavity
Due to incomplete development of body compartments
Agenesis of the heart (acardia): Absence of heart. Not viable
Amorphus globosus: Spherical, covered in hair, acardiac monster attached to the placenta
by a cord in cows. Severely anomalous second fetus
Patent ductus arteriosus:
This vascular channel between the pulmonary artery and aorta allows blood to bypass the lung during fetal life, converted to the solid ligamentum arteriosum postnatally, maybe patent but functionally insignificant in neonatal animals When persistent, blood is shunted from the left to the right side resulting in pulmonary hypertension
Poodles, Collie, Pomeranian, Chihuahua, Maltese, English springer spaniel, Shetland Sheepdog
Atrial septal defects
failure of closure of foramen ovale - interatrial - septal shunt that allows blood to bypass the lungs of the fetus
doberman, pinscher and samoyed
true septal defect: faulty development of the interatrial septum
ventricular septal defect
Failure of closure of interventricular septum
Bulldog, Springer spaniel
and West Highland white terrier
shunt left-to-right
equal ventricular pressures
pressure hypertrophy of the right ventricle
volume hypertrophy of the left ventricle
Semilunar valve stenoses
supravalvular
valvular
subvalvular
circuferential band of fibrous or muscular tissue
above, below or at level of valve
Pulmonic stenosis:
Usually valvular lesions.
• Pressure overload → concentric hypertrophy (right)
• Roughening, deformation and dilation of the surface of the pulmonary artery (jet like lesions).
• Beagle, Bulldog and Chihuahua.
Tetralogy of Fallot
Complicated cardiac anomaly with four lesions
Ventricular septal defect (A)
2 .Pulmonic stenosis (B)
Dextroposition of the aorta (C)
Secondarily- Hypertrophy of the right ventricular myocardium
Bulldog and Keeshond
Clinical – Cyanosis (similar to “Blue baby syndrome” in humans)
Valvular haematomas:
Haematocyst or lymphocysts on atrioventricular valves in ruminants
regress spontaneously and cause no functional abnormalities
Persistent right aortic arch:
The right fourth aortic arch, rather the left, develops and ascends on the right side of the midline
The ligamentum arteriosum forms a vascular ring over the oesophagus and the thrachea
Oesophageal obstruction and proximal dilation, megaoesophagus -> regurgitation
German shepherd, Irish setter and Great Dane
Valvular agenesis / hypoplasia
Peritoneopericardial diapragmatic hernia: Dogs with imcomplete development of the diaphragm. Abdominal viscera can be located in the pericardial sac
parasites
tumours
Pathophysiological mechanisms of
cardiovascular dysfunction (heart failure)
Pump failure - weak contractility, myocardial disease
Obstruction of flow - valvular stenoses, vascular narrowing
Regurgitant flow - valvular dysfunction
Shunted flow - congenital defects
Ruptures - heart wall, major vessels
Conduction disorders
clinical signs
Cardiac syncope (fainting / loss of consciousness):
Massive myocardial necrosis, ventricular fibrillation, arrythmias and reflex cardiac
inhibition (intestinal volvulus).
Congestive heart failure:
slow, gradual loss of pumping ability
• pressure (hypertension or stenosis),
•volume (fluid overload)
•mild myocardial damage (infarction).
Reduced renal blood stimulates renin-angiotensin-aldosterone system
sodium and water retention
•Increased plasma volume and increase the workload on the already failing heart
response
cardiac dilation
• hypertrophy
• decompensation
• death from cardiac failure
Left side heart failure
Subacute (pulmonary congestion and oedema)
Chronic (pulmonary congestion, oedema, fibrosis and haemosiderosis
(heart failure cells)
Cardiomyopathies, dysfunction of aortic and mitral valves
Right side heart failure
Subacute (passive congestion with hepatomegaly and splenomegaly)
Chronic (nutmeg liver and systemic oedema)
Myocardiopathies, pulmonary hypertension and dysfunction of tricuspid
and pulmonary valves
post mortem
blood clotting - red clots in the atria, right ventricle and large
vessels at the base of the heart
rigor mortis - occurs in the left myocardium and produces contracted rigid ventricular walls - less pronounced in right side of heart
Chicken fat clots
sedimentation of erythrocytes (or severe anaemia)
• clot consists of colourless fibrin
Haemoglobin imbibition
Postmortem lysis of erythrocytes produces diffuse red staining
of the endocardium
Barbiturate crystals
The intracardiac injection of euthanasia solution and other
substances can lead to the presence of crystalline deposits
vascular system/circulatory
haemorrhage
Frequent lesion in endocardium, myocardium and pericardium
Petechiae, ecchymoses or suffusive; in animals dying from septicaemia endotoxaemia, anoxia or electrocution
Horses: Very common agonal change
Pigs: Mulberry heart disease (vit E/Se deficiency) in growing pigs.
layers
peri and epi cardium
pericardial fluid
normal: clear, viscous, lubricating
pneumopericardium
hydropericardium
chylopericardium
haemopericardium
other/further pericardial alterations
endocardium
myocardium, cardiomyopathies
normal form and function
embryology
Heart develops from splanchnic mesenchyme in the cardiogenic area
single heart tube (primitive heart).
cardial looping turns it from a tube to a c-shape chamber
Surrounding mesenchyme thicken to form the myoepicardial mantle
The future heart develops dilatations and constrictions resulting in 4 chambers:
sinus venosus
primordial atrium
primordial ventricle
bulbus cordis
septum secundum is an incomplete partition and leaves a foramen ovale
Before birth the foramen ovale allows blood to pass from the right into the left atrium
anatomy
layers of heart
endocardium, myocardium, epicardium, pericardium
physiology
histology
myocardium
purkinje fibres, muscle, striations, centrally-placed nuclei, capillaries
histopathology
A small lesion in the conduction system can be fatal, whereas a widespread myocardial lesion
can be asymptomatic